The observation of accelerated atherosclerosis and thrombosis in children suffering from homocystinuria has resulted in studies which suggest a role for altered homocystine metabolism in the pathogenesis of atherosclerosis. We believe that any study of disorders in the metabolism of sulfur amino acids cannot be separated from or unrelated to the study of the metabolism of serine. The altered sulfur amino acids metabolism and increase in the incident of atherosclerosis is similar to the symptoms in women taking oral contraceptive hormones. Since the known enzymatic deficiencies associated with homocystinuria and the effects of oral contraceptive hormones both involve pyridoxal and folate metabolism our studies may help to clarify these relationships and the role of mammalian enzymes involved in the metabolism of serine. The target enzymes are serine-threonine dehydratase, serine transhydroxymethylase and methylenetetrahydrofolate reductase.